Abstract
We delineated the role of Ca<sup>2+</sup>-activated K<sup>+</sup> channels in the phenomenon of spike frequency adaptation (SFA) exhibited by neurons in the caudal region of nucleus tractus solitarius (cNTS) using intracellular recording coupled with the current-clamp technique in rat brain slices. Intracellular injection of a constant depolarizing current evoked a train of action potentials whose discharge frequency declined rapidly to a lower steady-state level of irregular discharges. This manifested phenomenon of SFA was found to be related to extracellular Ca<sup>2+</sup>. Low Ca<sup>2+</sup> (0.25 mM) or Cd<sup>2+</sup> (0.5 mM) in the perfusing medium resulted in a significant increase in the adaptation time constant (τ<sub>adap</sub>) and an appreciable reduction in the percentage adaptation of spike frequency (F<sub>adap</sub>). In addition, the evoked discharges were converted from an irregular to a regular pattern, accompanied by a profound increase in mean firing rate. Intriguingly, similar alterations in τ<sub>adap</sub>, F<sub>adap</sub>, discharge pattern and discharge rate were elicited by apamin (1 μM), a selective blocker for small-conductance Ca<sup>2+</sup>-activated K<sup>+</sup> (SK) channels. On the other hand, charybdotoxin (0.1 μM), a selective blocker for large-conductance Ca<sup>2+</sup>-activated K<sup>+</sup> channels, was ineffective. Our results suggest that SK channels of cNTS neurons may subserve the generation of both SFA and irregular discharge patterns displayed by action potentials evoked with a prolonged depolarizing current.
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